Evidence map›Paper›PMID 27040987›Full record

ArticleScientific reports2016

A novel non-canonical Notch signaling regulates expression of synaptic vesicle proteins in excitatory neurons.

Yukari Hayashi, Hiroshi Nishimune, Katsuto Hozumi, Yumiko Saga, Akihiro Harada, Michisuke Yuzaki, Takeshi Iwatsubo, Raphael Kopan, Taisuke Tomita

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.9field-weighted citation impact, top 24% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed, 20 citations in OpenAlex.

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  2. Deficiency ofProceedings of the National Academy of Sciences of the United States of America · 2024
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 8 institutions in 2 countries.

Yukari HayashiLaboratory of Neuropathology and Neuroscience, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo 113-0033, Japan.
Hiroshi NishimuneDepartment of Anatomy and Cell Biology, University of Kansas Medical School, Kansas City, KS 66160, USA.
Katsuto HozumiDepartment of Immunology, Tokai University School of Medicine, Kanagawa 259-1193, Japan.
Yumiko SagaDivision of Mammalian Development, National Institute of Genetics, Shizuoka 411-8540, Japan.
Akihiro HaradaDepartment of Cell Biology, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan.
Michisuke YuzakiDepartment of Physiology, School of Medicine, Keio University, Tokyo 160-8582, Japan.
Takeshi IwatsuboDepartment of Neuropathology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-0033, Japan.
Raphael KopanDepartment of Developmental Biology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Taisuke TomitaLaboratory of Neuropathology and Neuroscience, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo 113-0033, Japan.
Keio University · JPCincinnati Children's Hospital Medical Center · USOsaka University · JPThe Graduate University for Advanced Studies, SOKENDAI · JPThe University of Tokyo · JPTokai University · JPUniversity of Kansas · USWashington University in St. Louis · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Notch signaling plays crucial roles for cellular differentiation during development through γ-secretase-dependent intramembrane proteolysis followed by transcription of target genes. Although recent studies implicate that Notch regulates synaptic plasticity or cognitive performance, the molecular mechanism how Notch works in mature neurons remains uncertain. Here we demonstrate that a novel Notch signaling is involved in expression of synaptic proteins in postmitotic neurons. Levels of several synaptic vesicle proteins including synaptophysin 1 and VGLUT1 were increased when neurons were cocultured with Notch ligands-expressing NIH3T3 cells. Neuron-specific deletion of Notch genes decreased these proteins, suggesting that Notch signaling maintains the expression of synaptic vesicle proteins in a cell-autonomous manner. Unexpectedly, cGMP-dependent protein kinase (PKG) inhibitor, but not γ-secretase inhibitor, abolished the elevation of synaptic vesicle proteins, suggesting that generation of Notch intracellular domain is dispensable for this function. These data uncover a ligand-dependent, but γ-secretase-independent, non-canonical Notch signaling involved in presynaptic protein expression in postmitotic neurons.

Indexed as

AnimalsCells, CulturedCoculture TechniquesMiceMitosisNeuronsNIH 3T3 CellsReceptors, NotchSignal TransductionSynaptic VesiclesSynaptophysinUp-RegulationVesicular Glutamate Transport Protein 1Receptors, NotchSlc17a7 protein, mouseSynaptophysinSyp protein, mouseVesicular Glutamate Transport Protein 1

Identifiers

PMID27040987
PMCPMC4819173
OpenAlexW2342154891

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.